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A Case Study of Negative Pressure Wound Therapy to Manage Acute Necrotizing Fasciitis
Necrotizing fasciitis is a devastating infection of the subcutaneous tissue. Without prompt diagnosis and surgical debridement, the infection can lead to large open wounds, amputations, and even death. Standard treatment involves surgical debridement to remove all involved necrotic and vascularized tissue, intravenous antibiotic treatment, hyperbaric oxygen (HBO) therapy to provide an aerobic environment that may decrease the virulence and tissue destruction, and wound care.1,2
After the necrotizing fasciitis is addressed and the patient is medically stable, attention can focus on healing the debrided wound. Options for wound closure include split-thickness skin grafting, delayed surgical closure, or healing by secondary intention. The latter is the only option when a patient refuses additional surgical treatment or is no longer a surgical candidate. This case study demonstrates the use of externally applied negative pressure wound therapy (NPWT) as a treatment alternative for managing the closure of a wound resulting from acute necrotizing fasciitis.
Case Report
History and diagnosis. Ms. S, a 45-year-old Hispanic woman with adult-onset diabetes, presented to the emergency department complaining of swelling and blistering of her left upper arm. Five days before admission, she had undergone umbilical hernia repair at a facility in another country and received IV antibiotics in her left hand. She did not report a history of fever or chills. Outpatient medications included pioglitazone and omperazole. On physical examination, Ms. S had a temperature of 99º F and her left upper extremity had areas of dusky bullous lesions and erythema (see Figure 1). Her hand was neurovascularly intact. Her white blood count was 12.4 with a differential of 79% neutrophils, 13% lymphocytes, 1% monocytes, and 4% bands. An x-ray of the left upper extremity demonstrated the presence of extensive subcutaneous air (see Figures 2, 3, 4). She received IV ceftriaxone and clindamycin and the orthopedic team was consulted. Based on the clinical examination, Ms. S was diagnosed as having necrotizing fasciitis of the left upper extremity.
Treatment. Ms. S was immediately taken to the operating room for surgical management. When the skin was opened on the volar and dorsal aspect of the left hand and forearm, a significant amount of subcutaneous air and foul-smelling fluid was expressed from the subcutaneous compartments (see Figure 5). Following the procedure, wet-to-dry dressings were applied to the wound bed. Ms. S was admitted to the ICU and started on IV nafcillin. Hyperbaric oxygen was not available at the facility. Ms. S recovered well and was transferred to the orthopedic surgery floor on post-op day 1 and clindamycin was added to her antibiotic treatment. An infectious disease specialist was consulted and concurred with the antibiotic treatment regimen.
On postoperative day 6, evidence of resuming infection of the left upper extremity wounds was noted. Ms. S was taken back to the operating room for further debridement and irrigation (see Figures 6, 7, 8). Anaerobic culture of the wounds eventually demonstrated the Gram-positive bacillus Clostridium perfringens. After the second procedure, the decision was made to use NPWT (V.A.C.® Therapy System, KCI, San Antonio, Tex) to treat the wounds. After these interventions, Ms. S had an uneventful recovery. She was discharged 24 days following admission with the NPWT device in place. Follow-up appointments were scheduled in the orthopedic and wound care clinics. A split-thickness skin graft, performed on an outpatient basis, was planned.
Negative pressure wound therapy applied to Ms. S’s extensive wounds helped facilitate healing. When offered a split-thickness skin graft, she refused the procedure. She continued to utilize NPWT, requesting removal 3 months after her discharge from the hospital. When NPWT was discontinued, the only remaining open wound was on the dorsal aspect of her left forearm (see Figure 9). Wound closure was facilitated with general wound care. Occupational therapy begun the following day primarily for education and wound care; range-of-motion exercises were continued to return left upper extremity function. At the final follow-up visit 63 weeks after the final operation, Ms. S had recovered full range of motion in her left elbow and her forearm wound nearly was closed and still undergoing epithelialization (see Figure 10).
Prognosis. Ms. S’s prognosis is good for recovery from this devastating, life-threatening infection, considering concern about treatment compliance. Her clinicians believe that split-thickness skin grafting to her left upper extremity wound would have facilitated recovery.
Discussion
Necrotizing fasciitis is an aggressive soft tissue infection that requires immediate diagnosis followed by aggressive surgical debridement and treatment.1,3 Although such infections can occur anywhere in the soft tissues, they have a predilection for the abdomen, perineum, and lower extremities. Many predisposing factors can lead to necrotizing fasciitis but the etiology is often unknown2,3 (see Table 1). Because this infection spreads so rapidly and the initial clinical signs are so subtle, it is imperative for clinicians to maintain a high index of suspicion.2 Clinically, acute necrotizing soft tissue infections present with wound pain out of proportion to obvious injury; tachycardia with unexplained fever; crepitus; foul, watery wound discharge; and skin blistering that may rapidly progress to septic shock.1,2
Knowing the patient’s history is important for making the final diagnosis of necrotizing fasciitis. A history of recent trauma (particularly vehicular or agricultural accidents with open fractures), crush injuries, elective or emergent surgery (especially intestinal procedures), intravenous drug abuse, or injury should increase the level of suspicion that necrotizing fasciitis may cause the presenting symptoms and should be included on the list of differential diagnoses.2
Immunologically compromising clinical states such as diabetes also may contribute to the development of necrotizing fasciitis. Radiological studies may demonstrate subcutaneous gas, a classic sign of these infections; however, absence of gas does not rule out infection.1
Common signs of Clostridial fasciitis include pain that is frequently intense and persistent, edema, and skin over the infected soft tissue that appears pale and then bronze.2 Blebs and hemorrhagic bullae can follow and often indicate systemic involvement.2 Subcutaneous gas formation may be palpated as crepitus or may be apparent on radiographs, as in this patient. In addition, a release of gas on entering the subcutaneous compartment is common.
These lethal soft tissue infections are caused by single or (more often) multiple organisms.1 For example, Clostridium and group A Streptococcus are responsible for monomicrobial necrotizing infections.1 On the other hand, polymicrobial infections may consist of both aerobic and anaerobic streptococci, coagulase-negative and coagulase-positive staphylococci, facultative and aerobic Gram-negative bacillus such as Bacteroides species, and Clostridium species.
Muscle destruction is apparent when the skeletal muscle initially appears edematous, pale, and gray, progressing to brick red and finally to green-purple or even black.1,2 This condition, necrotizing myonecrosis, is a specific type of necrotizing fasciitis caused by the Gram-positive spore-forming bacillus, C. perfringes.1 This organism causes rapid, devastating soft tissue necrosis with minimal clinical signs and typically produces life-threatening systemic symptoms.2 Aggressive surgical debridement is a vital component of therapy for individuals with this illness.1,2 Debridement of the involved tissues, including the muscle, is required.
The potential for devastating and permanent complications exists, especially if treatment is delayed. Morbidity and mortality can be significant. Tang et al4 evaluated 24 patients with necrotizing fasciitis; surgical procedures included two disarticulations, nine amputations, and 12 radical debridements; one patient had no procedure performed. Overall, the survival rate was 67%. As this study highlights, the effects of necrotizing fasciitis are serious and may include wide local excision of soft tissue, possibility of amputation, or even death.
Perry’s review2 of gas gangrene and Urschel’s1 case series suggest that the standard of care for necrotizing fasciitis consists of aggressive debridement, antibiotic therapy, HBO, and wound management.1,2 Specifically, Urschel’s1 case series of soft tissue infections confirms that surgical debridement and antibiotic therapy is the standard of care for necrotizing fasciitis. Nouraei et al5 demonstrated the use of radical surgical debridement and antibiotic therapy in a case of a 32-year-old woman with cervicofacial necrotizing fasciitis. Furthermore, radical surgical debridement was the initial treatment in nine patients diagnosed with necrotizing fasciitis in a case study review by Copson.6 In Tang et al’s4 retrospective review, surgical debridement and antibiotic therapy were the initial management regimens.
Negative pressure wound therapy provides another adjunctive management option to help close wounds caused by necrotizing fasciitis. Morykwas et al7 used a pig model to examine four individual physiologic responses of wound healing to NPWT: 1) the effect of subatmospheric pressure on laser Doppler-measured blood flow in the wound and adjacent tissue (n = 5), 2) the rate of granulation tissue formation (n = 10), 3) clearance of bacteria from infected wounds (n = 5), and 4) measurement of nutrient flow by random-pattern flap survival (n = 5). Their study showed that, in animal models, NPWT enhances blood flow to and from the wound bed four-fold. Also, a significant difference (P ≤0.05) was noted in the proliferation of granulation tissue and tissue bacterial counts decreased (P ≤0.05) within 4 days of NPWT. Specifically, the number of micro-organisms per gram of tissue in contaminated wounds and the vascularity and development of granulation tissue exhibited an inverse relationship — micro-organism counts decreased while vascularity and granulation tissue increased. Likewise, bacterial count was observed to decrease to as low as 102 per gram of tissue from an initial level of approximately 108 per gram of tissue. Successful healing of skin grafts has been correlated with bacterial counts less than 105 per gram of tissue.8
Using NPWT for wound management was found to be superior to wet-to-dry dressings in a pilot study of 10 patients with postoperative diabetic foot wounds.9 Wounds treated with NPWT closed, on average, 3 weeks sooner than wounds treated with wet-to-dry saline-moistened dressings; however, due to the small sample size, statistical analysis was not performed.
Joseph et al10 randomly assigned 24 patients with 36 chronic, nonhealing wounds to NPWT or control treatment with saline wet-to-dry dressings. Wound bed depth in patients receiving NPWT decreased 66% versus 20% in the control group (P ≤0.00001). The authors concluded that the NPWT group demonstrated increased vascularity (angiogenesis) and rate of granulation tissue formation. Argenta and Morykwas11 retrospectively reviewed their clinical experience using NPWT in 175 chronic wounds, 94 subacute wounds, and 31 acute wounds. The authors observed an increase in the rate of granulation tissue formation in acute wounds — soft tissue avulsions, contaminated wounds, hematomas, and eviserations — compared to chronic and subacute wounds. This change was consistent with a decrease in wound size. Most acute wounds had extensive edema and contamination and large volumes of edematous fluid were removed from these wounds. One case described the removal of 4 L of fluid from a traumatic hip disarticulation wound without changes in hemodynamic status. The case study by Nouraei5 describes the copious amounts of exudative drainage. Furthermore, NPWT has been demonstrated to facilitate closure of various infected wounds. DeMaria et al12 used NPWT to treat an infected groin wound with a patent reverse saphenous vein femoropoliteal bypass graft in the wound bed. Likewise, Gustafsson et al13 retrospectively studied 40 consecutive patients with deep sternal wound infections that were treated with NPWT; their investigation supported use of NPWT as an alternative treatment for these infections because it facilitated removal of bacterial infection and provided sternal bone sparing, ultimately allowing sternal refixation. In addition, a new technique for treating infected wounds —NPWT combined with instilled treatment solutions (wound instillation) — alternates negative pressure with delivery of treatment solutions to the wound bed. Wolvos’14 case series demonstrated a reduced bacterial load and reduced wound pain when antibiotic and anesthetic solutions were instilled into wounds infected with wet gangrene, osteomyelitis, oxacillin-resistant Staphylococcus aureus, and Pseudomonas aeruginosa.
Conclusion
Acute necrotizing fasciitis is a devastating infection that causes massive necrosis of tissues and requires immediate clinical diagnosis and treatment. The treatment is emergent surgical debridement followed by antibiotic therapy, HBO, and wound care. Surgical closure is the optimal treatment to cover these wounds; however, as this case study demonstrates, NPWT may provide an alternative or adjunctive therapy choice for patients unable or unwilling to return to the operating room for additional surgical procedure.
The safety and effectiveness of NPWT as a treatment for closure of wounds contaminated with C. perfringens has not been studied. In this case, no adverse events occurred and NPWT facilitated primary closure of an upper extremity wound caused by acute necrotizing fasciitis. Prospective, controlled clinical studies involving NPWT in wounds caused by necrotizing fasciitis in the extremities are required to ascertain the efficacy of this therapy.
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